Lp(a) was firstly found in blood of patients suffering from arteriosclerosis and has been considered to be a fatal factor for arteriosclerosis. Today, it has been known as a kind of lipoprotein having apoprotein B-100 (the same as LDL molecule) at the central part to which apoprotein (a) is bonded. (cf. Gendai Iryou, vol.22, no.7, 1990).
Lp(a) is detected only in Primates including human being. Therefore, it is difficult to subject to animal experiment using rodents and the like whereby its investigation of its behavior in animals has been delayed.
Lp(a) has the same fundamental structure as plasminogen and, accordingly, Lp(a) is supposed to participate in inhibition of decomposition of fibrin in blood resulting in inhibition of dissolution of thrombosis.
Lp(a) is distributed in the area where arteriosclerosis may take place in higher concentrations than other areas whereby Lp(a) is presumed to directly participate in arteriosclerosis. In addition, the concentration of Lp(a) in blood is not affected by conventional hypolipemic drugs and arteriosclerosis is observed even in the people with low lipid level. Consequently, the relation between Lp(a) and arteriosclerosis has been considered to be important.
It has been known that the Lp(a) of the patients of arteriosclerosis and hyperlipemia never lowers in blood by a diet therapy.
It has been known that high Lp(a) concentration in blood is dominated and decided by genetic factor.
Out of the above-given knowledges, it may be easily concluded that Lp(a) is directly related to arteriosclerosis and is based upon the inhibitory action of dissolution of thrombosis.